| Project/Area Number |
16K19461
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAHASHI MOTOKO 札幌医科大学, 医学部, 教授 (00303941)
TAKAHASHI HIROKI 札幌医科大学, 医学部, 教授 (60231396)
SAKUMA YUJI 札幌医科大学, 医学部, 准教授 (10364514)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 肺サーファクタント蛋白質D / 変異型EGFR / 肺がん / 糖鎖 / レクチン / 肺サーファクタントタンパク質 / EGFR遺伝子変異 / 肺サーファクタント蛋白質 / EGFR / 肺サーファクタント / 肺コレクチン / SP-D |
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| Outline of Final Research Achievements |
We have previously demonstrated that SP-D suppressed wild-type EGFR signaling by blocking ligand binding to EGFR. Analysis of patients with lung adenocarcinoma to examine associations between serum SP-D levels and clinical outcome indicated that in TKI-treated patients with lung cancer harboring EGFR mutations, high serum SP-D levels correlated with prolonged overall survival. We herein demonstrate that SP-D downregulates ligand-independent signaling in cells harboring EGFR mutations. SP-D inhibits ligand-independent dimerization of EGFR mutants and dimerization-independent activation of EGFR mutants. SP-D augmented the viability-suppressing effects of EGFR-TKIs. It is possible that the suppressive effects of SP-D on EGF signaling might be implicated in improved clinical outcomes in patients with EGFR mutant lung cancer and high serum SP-D levels.
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